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RNA splicing is a key mediator of tumour cell plasticity and a therapeutic vulnerability in colorectal cancer

ABSTRACT: RNA splicing is a key mediator of tumour cell plasticity and a therapeutic vulnerability in colorectal cancer

PROVIDER: PRJNA820858 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18507000_1.fastq.gz	Fastqsanger.gz
	SRR18507000_2.fastq.gz	Fastqsanger.gz
	SRR18508200_1.fastq.gz	Fastqsanger.gz
	SRR18508200_2.fastq.gz	Fastqsanger.gz
	SRR18507001_1.fastq.gz	Fastqsanger.gz

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RNA splicing is a key mediator of tumour cell plasticity and a therapeutic vulnerability in colorectal cancer [wild-type and Apc mutant]

Project description:RNA splicing is a key mediator of tumour cell plasticity and a therapeutic vulnerability in colorectal cancer [wild-type and Apc mutant]

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RNA splicing is a key mediator of tumour cell plasticity and a therapeutic vulnerability in colorectal cancer [Apc mutant and Apc Srsf1 double mutant]

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RNA splicing is a key mediator of tumour cell plasticity and a therapeutic vulnerability in colorectal cancer.

Project description:Tumour cell plasticity is a major barrier to the efficacy of targeted cancer therapies but the mechanisms that mediate it are poorly understood. Here, we identify dysregulated RNA splicing as a key driver of tumour cell dedifferentiation in colorectal cancer (CRC). We find that Apc-deficient CRC cells have dysregulated RNA splicing machinery and exhibit global rewiring of RNA splicing. We show that the splicing factor SRSF1 controls the plasticity of tumour cells by controlling Kras splicing and is required for CRC invasion in a mouse model of carcinogenesis. SRSF1 expression maintains stemness in human CRC organoids and correlates with cancer stem cell marker expression in human tumours. Crucially, partial genetic downregulation of Srsf1 does not detrimentally affect normal tissue homeostasis, demonstrating that tumour cell plasticity can be differentially targeted. Thus, our findings link dysregulation of the RNA splicing machinery and control of tumour cell plasticity.

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RNA splicing is a key mediator of tumour cell plasticity and a therapeutic vulnerability in colorectal cancer

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RNA splicing is a key mediator of tumour cell plasticity and a therapeutic vulnerability in colorectal cancer [wild-type and Apc mutant]

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Chemotherapy induces cell plasticity; controlling plasticity increases therapeutic response.

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Project description:Cancer cell plasticity due to the dynamic architecture of interactome networks provides a vexing outlet for therapy evasion. Here, through chemical biology approaches for systems level exploration of protein connectivity changes applied to pancreatic cancer cell lines, patient biospecimens, and cell- and patient-derived xenografts in mice, we demonstrate interactomes can be re-engineered for vulnerability. By manipulating epichaperomes phar- macologically, we control and anticipate how thousands of proteins interact in real-time within tumours. Further, we can essentially force tumours into interactome hyperconnectivity and maximal protein-protein interaction capacity, a state whereby no rebound pathways can be deployed and where alternative signalling is supressed. This approach therefore primes interactomes to enhance vulnerability and improve treatment efficacy, enabling therapeutics with traditionally poor performance to become highly efficacious. These findings provide proof-of-principle for a paradigm to overcome drug resistance through pharmacologic manipulation of proteome-wide protein-protein interaction networks..

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